Journal
CLINICAL SCIENCE
Volume 119, Issue 7-8, Pages 353-359Publisher
PORTLAND PRESS LTD
DOI: 10.1042/CS20100151
Keywords
gene variant; myocardial infarction; urokinase-plasminogen activator (uPA); urokinase-plasminogen activator receptor (uPAR)
Categories
Funding
- Ministry of Science and Technology of China
- National High-tech Research and Development Program of China [2006AA02A406]
- International Science and Technology Cooperation Program of China [2009DFB30050]
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uPA (urokinase-plasminogen activator) and its receptor (uPAR) have been implicated in a broad spectrum of pathophysiological processes, including fibrinolysis, proteolysis, inflammation, atherogenesis and plaque destabilization, all of which are involved in the pathogenesis of MI (myocardial infarction). We hypothesized that putative functional genetic variation in the two genes encoding uPA and uPAR (PLAU and PLAUR respectively) might influence the susceptibility to MI. We genotyped rs4065 [3'-UTR (untranslated region) *141C > T) and rs2227564 (Pro 141 Leu) in the PLAU gene as well as rs34478 I (-5I6T > C) in the PLAUR gene in 633 MI patients and 1237 gender- and age-matched control subjects. Our results showed that the T allele of rs4065 was significantly associated with an increased risk of MI, with an adjusted OR (odds ratio) of 1.38 [95% CI (confidence interval), 1.07-1.78; P = 0.012) under the dominant model, 1.4 (95% CI, 1.12-1.75; P=0.003) under the additive model and 2.5 (95% Cl, 1.15-5.41; P = 0.02) under the recessive model. The findings were then replicated in another independent case-control study including 545 MI patients and 597 control subjects. In conclusion, our results suggest that rs4065 might be a previously unknown genetic risk factor for MI in the Chinese Han population.
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